A wide assortment of implantable medical devices (IMDs) are presently known and in commercial use. Such devices include cardiac pacemakers, cardiac defibrillators, cardioverters, neurostimulators, and other devices for delivering electrical signals to excitable tissue and/or receiving signals from the tissue. Devices such as pacemakers, whether implantable or temporary external type devices, are part of a system for delivering an electrical therapy or monitoring a patient condition. In addition to the pacemaker device, which typically has some form of pulse generator, a pacing system includes one or more leads carrying electrodes for delivering generated stimulation pulses to the heart and for sensing cardiac signals.
Pacemakers treat heart conditions in which the heart beats at a rate that is considered to be too slow, commonly referred to as bradycardia, by sensing cardiac signals and delivering appropriately timed electrical stimulation pulses to the atria and/or ventricles as needed to cause the myocardium to contract. Pacemakers may sense intrinsic cardiac signals that occur when the myocardium depolarizes naturally, causing a normal myocardial contraction or heart beat. A sensed signal associated with ventricular contraction is referred to as an R-wave, and a sensed signal associated with atrial contraction is a P-wave. When an intrinsic R-wave or P-wave is not sensed by the pacemaker, a stimulation pacing pulse is delivered, eliciting an evoked response which causes the myocardium to contract, thus maintaining a desired heart rate.
Pacemakers operate in either a unipolar or bipolar mode, and pace the atria and/or the ventricles of the heart. Unipolar pacing requires a lead having only one distal electrode for positioning in the heart, and utilizes the case, or housing of the implanted device as the other electrode for the pacing and sensing operations. For bipolar pacing and sensing, the lead typically has two electrodes, a tip electrode disposed at the distal end of the lead, and a ring electrode spaced somewhat back from the distal end. Each electrode is electrically coupled to a conductive cable or coil, which carries the stimulating current or sensed cardiac signals between the electrodes and the implanted device via a connector.
Combination devices are available for treating both fast and slow cardiac arrhythmias by delivering electrical shock therapy for cardioverting or defibrillating the heart in addition to cardiac pacing therapies. Such a device, commonly known as an implantable cardioverter defibrillator or “ICD”, uses coil electrodes for delivering high-voltage shock therapies. An implantable cardiac lead used in combination with an ICD may be a tripolar or quadrapolar lead equipped with a tip electrode and a ring electrode for pacing and sensing functions and one or two coil electrodes for shock therapies.
In order to achieve stimulation or sensing in the right side of the heart, a lead may be positioned against the endocardium by advancing the lead through the vena cava into the right atrium for right atrial applications, or further advancing the lead into the right ventricle for right ventricular applications. In order to achieve stimulation or sensing in the left heart chambers, a lead, often referred to as a “coronary sinus lead,” may be positioned within the vasculature of the left side of the heart via the coronary sinus and great cardiac vein. This endovascular lead placement is sometimes referred to as “epicardial” placement since electrodes on a coronary sinus lead will sense or stimulate epicardial heart tissue.
In order to work reliably, cardiac leads need to be positioned and secured at a targeted cardiac tissue site in a stable manner. Unacceptable pacing or sensing thresholds measured during an implant procedure may require lead repositioning. Shifting or dislodgement of the lead over time may result in changing thresholds, sometimes requiring programming adjustments in order to maintain an appropriate level of therapy. At the same time, increased pacing thresholds decrease the useful life of the battery in the implantable device, requiring earlier device replacement. Poor or inaccurate sensing of naturally occurring heart signals may result in inappropriate withholding or delivery of therapy.
To address these problems, an electrode may be passively secured in a desired endocardial position by the use of tines located at the distal end of a lead. The tines engage with the endocardial trabeculae, holding the distal lead end in place. Alternatively, an electrode may be actively secured by the use of a rotatable fixation helix. The helix exits the distal end of the lead and can be screwed into the body tissue. The helix itself may serve as an electrode or it may serve exclusively as an anchoring mechanism to locate an electrode mounted on the lead adjacent to a targeted tissue site. The fixation helix may be coupled to a drive shaft that is further connected to a coiled conductor that extends through the lead body as generally described in U.S. Pat. No. 4,106,512 issued to Bisping et al. A physician rotates the coiled conductor at a proximal end to cause rotation of the fixation helix via the drive shaft. As the helix is rotated in one direction, the helix is secured in the cardiac tissue. Rotation of the fixation helix in the opposite direction removes the helix from the tissue to allow for repositioning of the lead at another location.
These fixation methods, however, are not entirely appropriate in left heart stimulation and sensing applications when the lead is positioned endovascularly. A helical coil would puncture a cardiac vein. Tines would make lead re-positioning difficult because retraction of a tined lead within a narrow vein could potentially damage the valves within the vein. Tissue encapsulation of various passive and active fixation devices is normally encouraged to further stabilize an endocardial lead position. Tissue encapsulation is undesirable in stabilizing an endovascular lead, however, since such tissue ingrowth may obstruct blood flow. Methods for stabilizing an endovascular lead must allow for unimpeded blood flow. One method for stabilizing an endovascular lead is disclosed in U.S. Pat. No. 6,161,029, issued to Spreigl, et al., and includes an expanded stent that is lodged against the blood vessel wall to inhibit movement of the stent and a distal electrode support. The expanded stent lumen is aligned with the electrode support lumen for allowing blood to flow through the aligned electrode support lumen and expanded stent lumen.
Another problem encountered in left heart stimulation is that conventional circumferential tip or ring electrodes on a coronary sinus lead will direct current in the direction of the adjacent epicardium but also in directions away from the targeted tissue, which may reduce stimulation efficiency. Stray current may also cause undesired extraneous stimulation, such as phrenic nerve stimulation or atrial stimulation during ventricular pacing. A coronary sinus lead would preferably direct current only in the direction of the targeted myocardium. Correctly positioning an endovascular lead having an electrode on only one side, however, would be difficult and time consuming.
Lead failure sometimes occurs when a conductor becomes fractured or the insulation between electrodes and/or conductors fails. A unipolar lead failure generally requires a surgical procedure to replace the failed lead. In the case of a bipolar lead, a bipolar stimulation or sensing configuration may be reprogrammed to unipolar if one electrode on the lead remains functional. However, the remaining functional electrode may be positioned at a different location relative to the targeted cardiac tissue and may not provide as effective or efficient sensing or stimulation as the bipolar pair. Furthermore, in some patients, unipolar sensing does not provide an acceptable signal-to-noise ratio.
For effective cardiac pacing, a delivered stimulation pulse must be of adequate energy to cause depolarization of the myocardium, referred to as “capture.” The lowest pulse energy that successfully captures the heart is referred to as the pacing threshold. In order to verify that a pacing pulse has captured the heart, modern pacemakers are equipped with automatic capture detection algorithms. Capture may be verified by various methodologies known in the art such as sensing for an evoked R-wave or P-wave after delivery of a pacing pulse, sensing for the absence of an intrinsic R-wave or P-wave during the refractory period after a pacing pulse, or detecting a conducted depolarization in an adjacent heart chamber. Various capture verification methods are described in U.S. Pat. No. 5,601,615 issued to Markowitz et al., U.S. Pat. No. 5,324,310 issued to Greeninger et al., and U.S. Pat. No. 5,861,012 issued to Stroebel, each of which patents are incorporated herein by reference in their entirety. If capture is not verified, the pacing pulse energy may be automatically increased.
An electrode configuration used for pacing and evoked response sensing for capture detection may utilize a bipolar lead on which a tip electrode provides unipolar pacing and the tip and ring electrode pair provide bipolar sensing of the evoked response. A limitation of using the same electrode for pacing and evoked response sensing is that the pacing pulse and ensuing after-potential and electrode-tissue polarization artifact mask the evoked response until they dissipate, after which the evoked response, if any, has typically passed the sensing electrodes. Therefore, it is desirable to use an electrode pair that does not include the pacing electrode for sensing an evoked response. To overcome the problems of after-potential and the electrode-tissue polarization artifact, capture verification methods have been proposed which involves sensing for a conducted depolarization at a site away from the pacing electrode. For example, sensing a ventricular depolarization after an atrial pacing pulse has been delivered is evidence that the atrium was captured and the evoked depolarization was conducted to the ventricle.
For accurate evoked response detection, however, it is desirable to sense the evoked response using a bipolar sensing electrode pair in the vicinity of the stimulated cardiac tissue site. Unipolar sensing or sensing in other areas of the heart could lead to erroneous evoked response detection due to noise or other myopotentials being sensed as an evoked response. Furthermore, sensing for an evoked response in another area of the heart may not be possible in patients having conduction disorders.
What is needed, therefore, is an improved lead design that allows accurate targeting of excitable tissue in both endovascular and endocardial applications. A lead having an electrode arrangement that allows for reliable pacing and evoked response sensing for the purpose of capture verification is also desirable. Such a lead must be stabilized in a way that, when used endovascularly, does not cause undue vessel damage during fixation or repositioning and allows for unimpeded blood flow. Furthermore, an improved lead design should provide for alternative stimulation or sensing configurations without compromising effectiveness and efficiency of therapy delivery in case one electrode fails.